Amyloid beta A4 protein (APP)

Links to databases

Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1. Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts. Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain. The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis. N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).

NOTE: The calibrator curve below shows the performance of the assay with the estimated sensitivity and dynamic range parameters indicated. These curves are generated during the assay validation process using recombinant antigens. Please note that when analyzing biological samples the data generated will be given in the form of relative quantification (NPX values) and cannot be converted to absolute protein concentrations. For more info about NPX measurements, please visit our FAQ page.

Analytical Measuring Range

Please note: the technical data reported below refers to the measured value in the in vitro validation assays. Since the Development panel uses human samples diluted 100-fold, a multiplication factor of 100 should be applied when comparing the addressable biological concentration to this validation data.

LOD (pg/mL)

244

LLOQ (pg/mL)

244

ULOQ (pg/mL)

250000

Hook (pg/mL)

250000

Range (logs)

3

Calibrator curve for validation data (generated in multiplex)

Precision

Within run precision Coefficient of Variation (CV)

9%

Between run precision Coefficient of Variation (CV)

8%

Precision (repeatability) is calculated from linearized NPX values over LOD.

Biomarker Validation Data

Additional validation data, as well as a more detailed description of how the Olink panels are quality controlled can be found in our Data Validation documents. To download or to learn more go to the Data Validation page.